Neurotrophin-evoked depolarization requires the sodium channel NaV1.9

Robert Blum, Karl W. Kafitz and Arthur Konnerth ()
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Robert Blum: Institut für Physiologie, Ludwig-Maximilians-Universität München
Karl W. Kafitz: Institut für Physiologie, Ludwig-Maximilians-Universität München
Arthur Konnerth: Institut für Physiologie, Ludwig-Maximilians-Universität München

Nature, 2002, vol. 419, issue 6908, 687-693

Abstract: Abstract Brain-derived neurotrophic factor (BDNF) and other neurotrophins are essential for normal brain function. Many types of neurons in the central nervous system are excited by BDNF or neurotrophin-4/5, an action that has recently been implicated in synaptic plasticity. The mechanisms involved in this transmitter-like action of neurotrophins remains unclear. Here, by screening candidate genes with an antisense messenger RNA expression approach and by co-expressing the receptor tyrosine kinase TrkB and various sodium channels, we demonstrate that the tetrodotoxin-insensitive sodium channel NaV1.9 underlies the neurotrophin-evoked excitation. These results establish the molecular basis of neurotrophin-evoked depolarization and reveal a mechanism of ligand-mediated sodium channel activation.

Date: 2002
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DOI: 10.1038/nature01085

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